The heart is a pump that pumps life-sustaining blood throughout the body of the patient. A good summary of how the heart performs its function of a pump, including a brief description of the physiology of the heart, may be found in U.S. Pat. No. 5,340,361, incorporated herein by reference.
A pacemaker is an implantable medical device that monitors the activity of the heart for the occurrence of P-waves and/or R-waves, and steps in with electronically generated stimuli, when needed, to force the depolarization of the atria and/or ventricles. A pacemaker-generated stimulus that is delivered to the atrium is referred to herein as an "A-pulse". A pacemaker-generated stimulus that is delivered to the ventricle is referred to herein as a "V-pulse". Most pacemakers are configured to provide an A-pulse and/or V-pulse only if a prescribed period of time has elapsed without the occurrence of a P-wave and/or an R-wave, i.e., without the occurrence of natural heartbeats.
The prescribed period of time used by the pacemaker between contraction of the ventricle and contraction of the atrium is generally referred to as the V-A Interval or the atrial escape interval. For most dual-chamber pacemaker modes of operation, only if a P-wave does not occur during the atrial escape interval will the pacemaker step in at the conclusion of such interval and generate an A-pulse.
The prescribed period of time used by the pacemaker between contraction of the atrium and contraction of the ventricle is referred to as the A-V Interval, or sometimes it is called the "AV Delay". The pacemaker, for most dual-chamber modes of operation, generates a V-pulse only if the AV Delay elapses without the occurrence of an R-wave.
In the above-described manner, the heart is thus afforded as much time as possible to beat on its own before the electronically-generated stimuli of the pacemaker are delivered to the heart, causing it to beat at the rate set by the pacemaker.
Heretofore, most cardiac patients using a pacemaker have suffered from at least one of various cardiac conditions or diseases that affect either the ability of the SA node to maintain and sustain a satisfactory heartbeat rate (hereafter "rate problems"), or the ability of the AV node or the AV bundle to conduct a suitable stimulus to the ventricle (hereafter "conduction problems"). Advantageously, both rate problems and conduction problems lend themselves well to a pacemaker solution because the underlying cardiac muscle tissue is in place and is capable of responding to the electronically-generated stimuli produced by the pacemaker.
In recent years, it has also been recognized that standard dual-chamber pacemakers can also be effective in treating individuals who have a primary abnormality of cardiac muscle function with totally normal rhythms. This is termed a cardiomyopathy. While there are subsets of cardiomyopathy, each of which has its own specific therapeutic regimens, dual-chamber pacing with a short AV delay intentionally resulting in a disordered sequence of ventricular activation, has been very effective in alleviating symptoms of chest pain, shortness of breath and syncope in patients with hypertrophic obstructive cardiomyopathy (HOCM) that has proven to be refractory to pharmacologic therapy.
In HOCM, there is a disproportionate thickening of the intraventricular septum resulting in a dynamic outflow tract obstruction with hypercontractility of the remaining muscle. This obstruction to the ejection of blood from the ventricle causes the heart muscle to work harder increasing its metabolic demand resulting in episodes of chest pain identical to angina pectoris but without concomitant atherosclerotic obstruction of the coronary arteries, shortness of breath or dyspnea and recurrent syncope. The primary therapy for this disorder is pharmacologic; using drugs which intentionally decrease the vigor of contraction. The net effect is that the degree of obstruction is reduced, improving the overall cardiac efficiency. Until recently, the only available option when pharmacologic therapy was no longer effective was an open heart operation to surgically excise a portion of the abnormally thickened muscular septum. As this is a procedure performed infrequently by most cardiac surgeons, the operative morbidity and even mortality was higher than for most cardiac operations. In recent years, it has been recognized that a disordered sequence of ventricular activation (as might occur with the spontaneous development of an intraventricular conduction abnormality called Left Bundle Branch Block (LBBB)) can delay the electrical activation of the intraventricular septum, referred to simply as the septum, thus delaying its mechanical contraction and reducing the outflow tract obstruction. The net effect is a reduction in the major symptoms associated with HOCM. In that a similar ventricular activation sequence can be induced by pacing from the right ventricular apex, dual-chamber pacing has been successfully employed to also treat these individuals who do not have any conduction system problem that would otherwise constitute a standard indication for pacing.
In accordance with the present invention, a dual-chamber pacemaker is implanted in patients suffering from HOCM and is programmed with a sufficiently short AV or PV interval to preempt the normal conduction pattern and initiate the desired disordered sequence of ventricular activation from the location of the ventricular pacing lead. During PV or AV pacing, the pacemaker delivers a V-pulse to the ventricles at a programmed delay after the occurrence of the atrial event, which atrial event could be either the occurrence of a P wave or the delivery of an A-pulse. With delivery of a V-pulse to the tissue before natural conduction is allowed to take place, the pacemaker causes electrical depolarization and resultant muscular contraction pattern that is different from the normal pattern. This altered mechanical contraction sequence, for many HOCM patients, advantageously results in a reduction in the degree of outflow tract gradient, improving cardiac output and reducing the work of the heart. The result is a reduction in the severity and incidence of the symptoms of chest pain, dyspnea and syncope.
PV or AV pacing is only effective, however, when the V-pulse is delivered to the ventricular tissue before the occurrence of an R-wave, i.e., before the ventricular tissue depolarizes. As soon as the ventricular tissue depolarizes, it becomes refractory, and will not respond to a V-pulse, until such time as it repolarizes. It is thus necessary, if AV or PV pacing is to be used, to set the AV (or PV) interval of the pacemaker to a value that is less than the patient's normal conduction time. Heretofore, this requirement has forced the AV (or PV) interval to be set to very short values, i.e., between 80 and 120 ms or shorter, because during exercise (or other periods of physical activity or physiological stress) the patient's native conduction time may shorten significantly. Thus, in order to guarantee that the pacemaker will always pace the ventricles (i.e., in order to assure that the V-pulse is delivered to the ventricular tissue at a time when it is not refractory), the AV (or PV) interval must be set to an interval that is shorter than any native conduction interval that might exist in the given patient at any given time.
Disadvantageously, setting a very short programmed AV (or PV) interval may adversely affect cardiac output because it may force ventricular contraction well before the ventricles have had sufficient time to be filled with blood from the atrium. Thus, what is needed for patients suffering from a HOCM is a pacemaker that paces the ventricles at a time in the cardiac cycle that is always less than the natural conduction time, i.e., at a time that is prior to the occurrence of an R-wave, but that is not so much less than the natural conduction. That is, what is needed is a pacemaker that automatically sets its internally-generated AV and/or PV intervals to be just short of the patient's native conduction time, thereby assuring that the AV (or PV) interval is sufficiently long to allow the blood to physically move from the atrium to the ventricles; yet remains sufficiently short to always be less than the patient's native conduction time, thereby assuring that the V-pulse is not delivered when the ventricular tissue is refractory.
Existing systems, see, e.g., U.S. Pat. No. 5,340,361, incorporated herein by reference, respond to a single sensed R-wave by shortening the subsequent AV or PV interval by a programmable interval or delta. However, an ectopic R-wave that fails to represent true conduction, but rather a coincidental event following a paced or sensed atrial event, will result in a shortening of the AV or PV interval for the ensuing 256 cycles. The shortened interval may be physiologically inappropriate and cause hemodynamic deterioration.
When the AV and/or PV interval is shortened to a value that is just less than the native conduction time, there is also a need to regularly check the interval to determine whether it is still set at a value that is just less than the patient's native conduction time. This is because the patient's native conduction time will normally change over a period of time and may increase without detection, leaving the conduction time too short. A particular stair-step searching technique for regularly checking the AV and/or PV interval to determine if it is still less than the native conduction time is described in U.S. Pat. No. 5,334,220, which patent is incorporated herein by reference. It would also be desirable to employ other techniques or systems wherein the AV or PV interval is always maintained at an interval that bears the prescribed relationship to the patient's natural conduction time, thereby obviating the need to periodically "search" for such an optimum value.
Some additional techniques known in the art for carrying out ventricular pacing, and in particular, for verifying the complete ventricular capture results from application of a V-pulse, are shown in U.S. Pat. Nos. 5,507,782 and 5,514,163.